126 results match your criteria: "University of Pennsylvania and The Children's Hospital of Philadelphia[Affiliation]"

Historically, complex metacarpophalangeal (MCP) joint dislocations have necessitated open surgical management by either a volar or dorsal approach. The authors describe a relatively simple and reliable percutaneous technique to treat these complex MCP dislocations, with results comparable with open surgical reduction. This minimally invasive technique can be performed in the emergency room setting, thereby avoiding the cost and morbidity associated with an open procedure in the operating room.

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SPECT scanning using (99)Tc-TRODAT-1, a ligand that binds to dopamine transporters, may be useful for detection of early Parkinson's disease (PD), diagnosis of presymptomatic individuals, and monitoring disease progression. Understanding whether genetic factors contribute to inter-individual variability is crucial for interpreting imaging results in the context of disease pathophysiology. We tested whether polymorphisms in the genes for catechol-O-methyltransferase (COMT), monoamine-oxidase B (MAO-B), and the dopamine transporter (DAT) influence dopamine uptake parameters in the striatum in vivo in asymptomatic volunteers and patients with PD as measured with (99)Tc-TRODAT-1.

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Hemophilia B is an X-linked coagulopathy caused by absence of functional coagulation factor IX (F.IX). Previously, we established an experimental basis for gene transfer as a method of treating the disease in mice and hemophilic dogs through intramuscular injection of a recombinant adeno-associated viral (rAAV) vector expressing F.

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Background: Friedreich ataxia is a progressive neurodegenerative disorder affecting afferent cerebellar pathways and other neuronal systems, including afferent visual pathways. A systematic clinical outcome measure for examination of visual dysfunction in Friedreich ataxia has not been identified. We sought to identify a simple, reliable method for assessing clinical and subclinical visual dysfunction in patients with Friedreich ataxia.

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Since excitotoxicity has been implicated in a variety of neuropathological conditions, understanding the pathways involved in this type of cell death is of critical importance to the future clinical treatment of many diseases. The N-methyl-D-aspartate (NMDA) receptor has become a primary focus of excitotoxic research because early studies demonstrated that antagonism of this receptor subtype was neuroprotective. However, initial pharmacological agents were not clinically useful due to the adverse effects of complete NMDA receptor blockade.

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The NMDA receptor is an important target for drug development, with agents from many different classes acting on this receptor. While the severe side effects associated with complete NMDA receptor blockade have limited clinical usefulness of most antagonists, the understanding of the multiple forms of NMDA receptors provides an opportunity for development of subtype specific agents with potentially fewer side effects. Different NMDA receptor subtypes are assembled from combinations of NR1 and NR2 subunits with each subunit conveying distinct properties.

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Endothelin-1 contributes to normocapnic hyperoxic pial artery vasoconstriction.

Brain Res

September 1999

Departments of Anesthesia and Pharmacology, University of Pennsylvania and The Children's Hospital of Philadelphia, 34th and Civic Center Blvd., Philadelphia, PA 19104, USA.

The present study was designed to determine if hyperoxia elicits pial artery vasoconstriction and to characterize the contribution of endothelin-1 (ET-1) to that vascular response in newborn pigs equipped with a closed cranial window. Hyperoxic conditions were established by ventilating the piglets with 100% O(2) during normocapnia and concomitantly topically applying artificial CSF that had been bubbled with 100% O(2). Hyperoxia elevated CSF ET-1 from 23+/-1 to 45+/-4 pg/ml.

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Screening of specific phage is often hampered by nonspecific binding either of the VCS M13 helper phage to the solid phase absorbent or to the polyclonal antibodies used for selection. The former is improved by increasing the stringency for selection. However, the available polyclonal anti-VCS M13 antibodies often react with immobilized antigen nonspecifically, making it difficult to distinguish between positive and negative clones.

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Previous studies observed that endothelin-1 (ET-1) contributed to ATP-sensitive K+ (K(ATP)) channel impairment 1 h following fluid percussion brain injury (FPI) in the newborn pig. The present study was designed to determine the effect of FPI on K(ATP) channel activity as a function of time in newborn (1-5 days old) and juvenile (3-4 weeks old) pigs equipped with a closed cranial window. FPI of moderate severity (1.

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Since recent studies show that pial artery dilation during a 20 or 40 min hypoxic exposure was less than that observed during a 5 or 10 min exposure, stimulus duration determines the nature of the vascular response to hypoxia. Decremented hypoxic pial dilation during longer exposure periods results, at least in part, from decreased release of methionine enkephalin (Met), an opioid known to contribute to dilation during hypoxia. Nitric oxide and cGMP contribute to both release and the vascular response to this opioid.

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BACKGROUND AND PURPOSE--Endothelin-1, in concentrations similar to that present in cerebrospinal fluid after fluid percussion brain injury (FPI), increases superoxide anion (O2-) production. Endothelin-1 also contributes to altered cerebral hemodynamics after FPI through impairment of ATP-sensitive K+ (KATP) channel function through protein kinase C (PKC) activation. Generation of O2- additionally occurs after FPI.

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Because pial artery dilation during a 20- or 40-min hypoxic exposure was less than that observed during a 5- or 10-min exposure, stimulus duration determines the vascular response to hypoxia. Dynorphin (Dyn) modulates hypoxic pial dilation and contributes to decremented dilation during longer hypoxic exposures. This study was designed to determine whether vasopressin (VP) contributes to Dyn modulation of hypoxic pial dilation in newborn pigs equipped with a closed cranial window.

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Nitric oxide contributes to opioid release from glia during hypoxia.

Brain Res

December 1998

Departments of Anesthesia and Pharmacology, University of Pennsylvania and The Children's Hospital of Philadelphia, Philadelphia, PA 19104, USA.

Activation of neuronal nitric oxide (NO) synthase contributes to increased CSF concentrations of the opioids methionine enkephalin and leucine enkephalin during hypoxia in the newborn pig. NO and these opioids, in turn, contribute to hypoxic pial artery dilation. However, the cellular site of origin for opioids detected in CSF cannot be determined using this in vivo model.

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Previous studies have observed that ATP- and calcium-sensitive K+ (KATP and Kca) channel function is impaired after fluid percussion brain injury (FPI). The present study was designed to characterize the effect of FPI on prostaglandin (PG)E2 and 12 pial artery dilation and the role of activation of these K+ channels in that dilation in newborn pigs equipped with a closed cranial window. FPI of moderate severity (1.

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Role of opioids in hypoxic pial artery dilation is stimulus duration dependent.

Am J Physiol

September 1998

Departments of Anesthesia and Pharmacology, University of Pennsylvania and The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104, USA.

Because methionine enkephalin contributes to and dynorphin opposes dilation during a 10-min hypoxic exposure, opioids modulate pial artery dilation to this stimulus. However, such modulation may be dependent on the duration of hypoxia. The present study was designed to characterize the modulation of hypoxic pial dilation by opioids as a function of stimulus duration in newborn pigs equipped with a closed cranial window.

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Although nitric oxide (NO) and calcium sensitive K+ channel (Kca) activation contribute to hypoxic pial artery dilation in the piglet, responses to the NO releasers SNP and SNAP are unchanged by the Kca channel antagonist iberiotoxin. These data suggest that NO does not elicit dilation via Kca channel activation. The present study was designed to determine if dilation by Kca channel activation is mediated by NO in newborn pigs equipped with a closed cranial window.

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Objectives: After fluid percussion brain injury (FPI) in the newborn pig, pial arteries constrict and responses to dilator stimuli, including opioids, are blunted. This study was designed to determine if altered release of prostaglandins contributes to blunted opioid dilation of cerebral arteries in newborn piglets following brain injury.

Design: Prospective, in vivo, cerebral hemodynamic animal study.

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Previous studies have shown that pial arteries constricted and responses to dilator opioids were blunted after fluid percussion injury (FPI) in newborn pigs. Membrane potential of vascular muscle is a major determinant of vascular tone and activity of K+ channels is a major regulator of membrane potential. Recent data show that opioids elicit dilation via the sequential production of cAMP and subsequent activation of calcium-sensitive K+ (K(Ca2+)) channels by this second messenger.

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Nitric oxide (NO) contributes to hypoxia-induced pial artery dilation, at least in part, via the formation of guanosine 3',5'-cyclic monophosphate (cGMP) and subsequent release of Met-enkephalin and Leu-enkephalin in the newborn pig. In separate studies, these opioids were also observed to elicit NO-dependent pial dilation. The present study was designed to investigate the role of the neuronal isoform of NO synthase (NOS) in hypoxic pial dilation, associated opioid release, and opioid dilation in piglets equipped with a closed cranial window.

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It has been previously observed that nitric oxide (NO) contributes to hypoxic pial artery dilation and that both sodium nitroprusside (SNP), a releaser of NO, and hypoxia elicit dilation via activation of ATP-sensitive K+ channels in the newborn pig. Other studies, however, have shown that NO activates calcium-sensitive K+ (K(Ca)) channels. The present study, therefore, was designed to investigate the role of K(Ca)-channel activation in NO and hypoxic dilation and to relate this mechanism to the previously observed role of NO in hypoxic dilation in newborn pigs equipped with closed cranial windows.

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IMMUNITY IN MUMPS : VI. EXPERIMENTS ON THE VACCINATION OF HUMAN BEINGS WITH FORMOLIZED MUMPS VIRUS.

J Exp Med

October 1946

School of Medicine of the University of Pennsylvania and the Children's Hospital of Philadelphia, Philadelphia, and the Department of Bacteriology and Immunology, Harvard Medical School, and the School of Public Health, Boston.

The results observed after experimental inoculation of active mumps virus into 41 vaccinated and 32 unvaccinated children,-with the consent of their parents or guardians,-indicated that formol-inactivated mumps virus obtained from the parotid gland of the infected monkey and employed as a vaccine in the manner which has been described increased the resistance of about half of those to whom it was administered.

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The results of skin tests read at 48 hours on several hundred adults and children in which heat-inactivated mumps virus was the antigen have been presented and discussed. They can be summarized as follows:- Of 89 persons tested before the onset of mumps, 89 per cent exhibited erythematous reactions 10 mm. or less in diameter and 95 per cent, reactions 15 mm.

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